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If it’s a vaccine, or similar to a vaccine, especially if it contains thimerosal you gotta figure someone, somewhere has blamed it as a cause of autism. Such is the case of anti-D immune globulins, like RhoGaM. RH-negative mothers are given these shots while pregnant to protect their RH-positive babies.

If you are thinking like I was at first, “RhoGaM…where I have heard this recently?”, probably the most famous case involving RhoGaM is that of the Sykes family in what became Sykes v. Bayer. This was blogged extensively at neurodiversity.com, including the recent dismissal of the suit. On the way, the Plaintiffs subpoenaed Ms. Seidel (the more than a mere mother who runs neurodiversity.com). Said subpoena was quashed, and Mr. Shoemaker, the attorney who subpoenaed Ms. Seidel was sanctioned for what was deemed a misuse of his powers as an officer of the court.

But, I digress…Back to RhoGaM and similar products.

Earlier this month, a study by Lisa Croen (and other people familiar in the epidemiology of autism) was published:

It’s worth reading, and, I would bet money, is soon to be attacked. Why? Take a look at the last line of the abstract:

“These data support previous findings that prenatal exposure to thimerosal-containing anti-D immune globulins does not increase the risk of autism. that prenatal exposure to thimerosal-containing anti-D immune globulins does not increase the risk of autism.”

One could speculate whether the parties in Sykes v. Bayer were aware that this paper was in press, and whether that had anything to do with the dismissal. Without any more information, it would be just that: speculation.

Something that rises above speculation, but is below the level of a conclusion of the paper is this question: does this mean that this level of thimerosal exposure to pregnant women (at least at the times similar to that of RhoGaM injections) is off the hook in general? Or, to put it more simply, does this tell us that thimerosal containing flu shots given to pregnant woman are likely not a contributor to autism risk?

This is an interesting question in some circles. In the shifting sands of the desert that is the thimerosal-caused-autism science, the thimerosal containing flu shot is gaining prominence. Ignore the fact that a minority of pregnant women get the flu shot. Somehow, these flu shots are supposed to be taking up the slack left behind by the phase out of thimerosal from the pediatric schedule. (I can hear people now, “oooh, he’s perpetuating the myth that thimersosal is gone. There are trace amounts left. Trace amounts!” Another of the sand-dunes of the desert.)

But, rest assured, Croen and company are aware of Dr. Geier’s team and included their work in their analysis.

Similarly, Geier and Geier found that the frequency of maternal Rh-negative status among 53 consecutive non-Jewish Caucasian patients with ASD referred to their genetic clinic was significantly higher than the frequency among 926 non-Jewish Caucasian pregnant women who presented at their clinic for prenatal genetic care (28.3% vs 14.4%, P ” .01), and all ASD patients with Rh-negative mothers received RhIg during pregnancy. Given the authors’ belief that thimerosal-containing vaccines cause autism, it is likely that the ASD patients who seek out their clinical services are skewed toward higher perceived mercury exposure. For that reason, these study findings may be biased and should be viewed with caution.

And, yes, they also note the Holmes “baby haircut“study as well. But that study has been through the wringer so many times, it’s best to move along.

Of course this isn’t going to be the end of the discussion. The Miles and Takahashi study was met in short order by a comment by Bernard, Blaxill and Redwood. I’d bet the cash in my wallet that a response to the Croen et al. study is in the works.

And, unfortunately, that is the problem we as a community have to deal with. As noted (with some sadness, I am sure) in the Omnibus testimony of Dr. Mumper, the question of thimerosal and autism is a closed book to the scientific community. There are a few studies still ongoing, but indications are that they will also show no effect.

It will be hard enough to keep the interest level high amongst legislators as the science quashes the guilt factor of vaccine induce autism. It will be even more difficult if we are perceived to be clinging to the failed theories and ignoring good science.

Autism isn’t “a novel form of mercury poisoning“. Not from vaccines, not from immune globulins, not from plumes of mercury from China. Let’s stop moving goalposts and patting ourselves on the back for being flexible. Instead, let’s accept that falsifiable hypotheses have had their chance and been falsified. That’s learning.

BACKGROUND: Immune dysfunction has been associated with autism, yet whether maternal immune status during pregnancy plays a causal role remains to be clarified. METHODS: We conducted a population-based case-control study nested within the cohort of infants born July 2000-September 2001 to women who participated in the prenatal screening program in Orange County, California. Cases (AU; n = 84) were children receiving services for autism at the Regional Center of Orange County. Two control groups were included: children with mental retardation or developmental delay (MR; n = 49) receiving services at the same regional center; and children not receiving services for developmental disabilities, randomly sampled from the California birth certificate files (GP; n = 160). Maternal autoantibody reactivity to fetal brain protein was measured by Western blot in archived mid-pregnancy blood specimens drawn during routine prenatal screening. Presence of specific bands and band patterns were compared between the three study groups. RESULTS: The pattern of maternal mid-gestation antibody reactivity to human fetal brain protein varied by study group and by autism onset type, although most differences did not reach statistical significance. Reactivity to a band at 39 kDa was more common among mothers of children with autism (7%) compared with mothers of MR (0%; p = .09) and GP control subjects (2%; p = .07), and simultaneous reactivity to bands at 39 kDa and 73 kDa was found only in mothers of children with early onset autism (n = 3). CONCLUSIONS: Our findings indicate that further studies of prenatal immune markers might be a productive area for etiologic and biologic marker discovery for autism.

the questions are not done considering the complexity of the current knowledge?
Why in this study again only numbers are only included? Who knows about the immune answer before and after the RhoGam- related to autoantibodies in the mothers of non-autistics vs mothers of autistic children- for example and others from the clinical point of view?

the study is aimed at peers/scientist and not the general public so only numbers are required… I’m really confused by the comment.

That said.

It gets me wondering. Lets say a reaction to vaccines did trigger autism. All this wasting time w/ thimerosal (sp?) would be drawing away from what it is about that reaction that triggered it… all the convincing vaccine stories have a kid with some violent reaction (per the listed side effects in the documentation), and symptoms of autism showed up after said violent reaction. Now that we’ve exhaustively shown no link btw mercury and autism, or even between mmr vaccine and autism, why do we need to harp on it? might it be more useful to figure out why the child had disabling symptoms after said reaction? You know, because maybe that might give us a clue to treatment methods, or even prevention? or is this an impossible thing to look into?

might it be useful to try to determine a way to predict who might have a potentially disabling reaction? because there’s no reason for a child that isn’t sensitive not to be vaccinated. (oddly enough, my autistic child is sensitive but had no reaction to his vaccinations, so sensitivity isn’t even a clear factor, I’ve posted on the comments here numerous times that his most marked regression came after walking and walking became a stim, rather than any environmental influence – ie his regression is probably because he learned to stim and wanted to stim above all else, kind of like when a beagle catches a scent and their ears no longer appear to work… – except I usually tend to say it this form: ‘Walking causes autism!’ just to be sarcastic…)

Is this because they really don’t want treatment? they really don’t want the cure they insist they want? Is it because all this fanfare over vaccines is because it gets the media to cover it and people to therefore fund it? or, well, fund research into it… You know, I might be a little more aligned with that logic if there was more research out there on treatments, and not just ABA, as even the proponents will acknowledge it doesn’t help every child. but so far I’ve found nothing reliable, and I have access to a university’s library databases. Granted, I’m not a librarian, but it does mean I have at my fingertips more than the average person and I don’t have to go into work (I work at said university’s library) to get it….

I am not sure if the Croen paper you cite is applicable here. There is no mention of RhoGaM or other immune globulins in that paper. The fraction of mothers that get them is low, so it isn’t likely a strong factor in the maternal antibodies study.

What does intrigue me about the Croen maternal antibodies study is that it doesn’t seem to fit with the Braunschweig paper from earlier this year (that also included Croen as an author).

We found, unlike the Braunschweig et al. study, that reactivity to the 39-kDa band was significantly more common among mothers whose children had early onset autism compared with control subjects, that reactivity to this band did not occur in any specimens from mothers of children with MR, and that reactivity to 39 kDa coupled with reactivity to 73 kDa was found only in the subgroup with early onset autism and not in either control population.

There were some significant differences in the studies (as noted by the authors). The largest being that the Croen study used samples taken during pregnancy, while the Braunschweig study used samples taken years later.

I am not aware of a case where a child had a “violent” reaction to a vaccine and was later found to be autistic. There are people who claim such things, but from what I have seen some of them provide no evidence at all, and what evidence is given is on a Yahoo! group or something. There were no such cases offered by the petitioners in the Omnibus Autism hearings. One would thing that if there was even one such case among the thousands of cases in the omnibus, that they’d have picked it as a good example of how vaccines cause autism.

I think it’s good to remember that not every person on the Internet who posts a story is telling any of the truth, or all of the truth.

Mrs Clark, you are not (aware) of this kind of cases. I am.
Sullivan, EXACTLy my point. These kind of aspects were not studied. now, How do we know IF RhoGAM has some kind of impact in autoimmunity if this aspect is not researched properly? For example how many children born from mothers immunized with RhoGAM have auto immune conditions and/or there are autoimmune conditions in the family?Are there adverse reactions to RhoGAM in mothers related to families with autoimmunity antecedents?Now, why – through what mechanism- are there autoantibodies to fetal Brain protein in the mother ?
Do you remember this

Brain Behav Immun. 2008 Feb 7.
Stereotypies and hyperactivity in rhesus monkeys exposed to IgG from mothers of children with autism.Martin LA, Ashwood P, Braunschweig D, Cabanlit M, Van de Water J, Amaral DG.
Department of Psychiatry and Behavioral Sciences, Center for Neuroscience, California National Primate Research Center and The M.I.N.D. Institute, University of California-Davis, 2825 50th Street, Sacramento, CA 95817, USA.Autism together with Asperger syndrome and pervasive developmental disorder not otherwise specified form a spectrum of conditions (autism spectrum disorders or ASD) that is characterized by disturbances in social behavior, impaired communication and the presence of stereotyped behaviors or circumscribed interests. Recent estimates indicate a prevalence of ASD of 1 per 150 (Kuehn, 2007). The cause(s) of most cases of ASD are unknown but there is an emerging consensus that ASD have multiple etiologies. One proposed cause of ASD is exposure of the fetal brain to maternal autoantibodies during pregnancy [Dalton, P., Deacon, R., Blamire, A., Pike, M., McKinlay, I., Stein, J., Styles, P., Vincent, A., 2003. Maternal neuronal antibodies associated with autism and a language disorder. Ann. Neurol. 53, 533-537]. To provide evidence for this hypothesis, four rhesus monkeys were exposed prenatally to human IgG collected from mothers of multiple children diagnosed with ASD. Four control rhesus monkeys were exposed to human IgG collected from mothers of multiple typically developing children. Five additional monkeys were untreated controls. Monkeys were observed in a variety of behavioral paradigms involving unique social situations. Behaviors were scored by trained observers and overall activity was monitored with actimeters. Rhesus monkeys gestationally exposed to IgG class antibodies from mothers of children with ASD consistently demonstrated increased whole-body stereotypies across multiple testing paradigms. These monkeys were also hyperactive compared to controls. Treatment with IgG purified from mothers of typically developing children did not induce stereotypical or hyperactive behaviors. These findings support the potential for an autoimmune etiology in a subgroup of patients with neurodevelopmental disorders. This research raises the prospect of prenatal evaluation for neurodevelopmental risk factors and the potential for preventative therapeutics.

The presence of a approximately 52 kDa MW band, in the plasma of subjects with AU, was detected with a significantly higher incidence when compared to plasma from TD controls (29% vs. 8%, P = 0.0027 and 30% vs. 11%, P = 0.01, in the thalamus and hypothalamus, respectively). Reactivity to three brain proteins (42-48 kDa MW), in particular in the hypothalamus, were observed with increased incidence in 37% of subjects with AU compared to 13% TD controls (P = 0.004).

Mrs Clark, you are not (aware) of this kind of cases. I am.
Sullivan, EXACTLy my point. These kind of aspects were not studied. now, How do we know IF RhoGAM-full composition-has some kind of impact in autoimmunity (even good or bad) if this aspect is not researched properly related to ASD? For example how many children born from mothers immunized with RhoGAM have auto immune conditions and/or there are autoimmune conditions in the family?Are there adverse reactions to RhoGAM in mothers related to families with autoimmunity antecedents?Now, why – through what mechanism- are there autoantibodies to fetal Brain protein in the mother ?
Do you remember this

Brain Behav Immun. 2008 Feb 7.
Stereotypies and hyperactivity in rhesus monkeys exposed to IgG from mothers of children with autism.Martin LA, Ashwood P, Braunschweig D, Cabanlit M, Van de Water J, Amaral DG.
Department of Psychiatry and Behavioral Sciences, Center for Neuroscience, California National Primate Research Center and The M.I.N.D. Institute, University of California-Davis, 2825 50th Street, Sacramento, CA 95817, USA.Autism together with Asperger syndrome and pervasive developmental disorder not otherwise specified form a spectrum of conditions (autism spectrum disorders or ASD) that is characterized by disturbances in social behavior, impaired communication and the presence of stereotyped behaviors or circumscribed interests. Recent estimates indicate a prevalence of ASD of 1 per 150 (Kuehn, 2007). The cause(s) of most cases of ASD are unknown but there is an emerging consensus that ASD have multiple etiologies. One proposed cause of ASD is exposure of the fetal brain to maternal autoantibodies during pregnancy [Dalton, P., Deacon, R., Blamire, A., Pike, M., McKinlay, I., Stein, J., Styles, P., Vincent, A., 2003. Maternal neuronal antibodies associated with autism and a language disorder. Ann. Neurol. 53, 533-537]. To provide evidence for this hypothesis, four rhesus monkeys were exposed prenatally to human IgG collected from mothers of multiple children diagnosed with ASD. Four control rhesus monkeys were exposed to human IgG collected from mothers of multiple typically developing children. Five additional monkeys were untreated controls. Monkeys were observed in a variety of behavioral paradigms involving unique social situations. Behaviors were scored by trained observers and overall activity was monitored with actimeters. Rhesus monkeys gestationally exposed to IgG class antibodies from mothers of children with ASD consistently demonstrated increased whole-body stereotypies across multiple testing paradigms. These monkeys were also hyperactive compared to controls. Treatment with IgG purified from mothers of typically developing children did not induce stereotypical or hyperactive behaviors. These findings support the potential for an autoimmune etiology in a subgroup of patients with neurodevelopmental disorders. This research raises the prospect of prenatal evaluation for neurodevelopmental risk factors and the potential for preventative therapeutics.

The presence of a approximately 52 kDa MW band, in the plasma of subjects with AU, was detected with a significantly higher incidence when compared to plasma from TD controls (29% vs. 8%, P = 0.0027 and 30% vs. 11%, P = 0.01, in the thalamus and hypothalamus, respectively). Reactivity to three brain proteins (42-48 kDa MW), in particular in the hypothalamus, were observed with increased incidence in 37% of subjects with AU compared to 13% TD controls (P = 0.004).

Until those “cases” are documented, they don’t really exist as far as I am concerned, as far as proving anything.

A child may be autistic, and may have a “violent” reaction to (correction) vaccines or a vaccine, but I have never ever seen any way for such a “violent” reaction to cause autism (or PDD,nos or Asperger’s), based on what I know about brain structure, brain function and autism.

Rarely a child may end up with brain damage, more or less random brain damage from a bad vaccine reaction, but it would be more or less random brain damage of the sort a kid gets from being bashed in the skull badly in an accident.

Sure, a kid, post brain trauma could act autistic, maybe, but it’s not the kind of autism we are usually thinking of when we talk about the majority of autistic people.

I’m a bit at a loss as to where you are going with this. I am aware of the other papers from the Braunschwieg study. I am aware of the “backflipping” monkey study by Amaral (I even have the videos downloaded).

But, my point is not exactly your point. My point is that these studies are not consistent yet, so trying to draw conclusions is premature. However the recent Croen study is consistent with the previous RhoGaM study, indicating that RhoGaM like products do not cause an increased risk of autism.

Perhaps you would like to say that no one has studied RhoGaM given to women with autoimmunity issues and seen if this increases the risk of autism?

Again, that is not exactly what I was saying. I was pointing out that there is an inconsistency between two of the maternal antibodies papers.

I would say that the papers you point to do not suggest a RhoGaM connection, as RhoGaM was not a part of the studies.

Actually, this would indicate to me that RhoGaM might be protective against autism as it would reduce immune response of an RH negative mother against an RH positive child.

Hi Sullivan
I apologize if I was not enough clear.It is not easy in spanish, in english is worse to be clear for me.
Thank you for your interest.I will explain you later what is my concerns on this topic- related to these manuscripts on RhoGam, autoimmunity and ASD.

Wouldn’t the incidence of Rh-neg mothers be going down though? I am one, but both of my children are positive (and I had Rhogam shots and thank God for them) – it would seem to me that in sheer numbers there is a shrinking pool of Rh-neg mothers anyway, soon to disappear entirely (in a few generations). So RH factor would have no impact on increasing autism incidence?

I have A+ blood, and hubby has A- blood. I did not have to worry about the incompatibility. But I would think my daughter would have about a 50/50 chance of having A- blood. (by the way, I checked PubMed, while I can find surveys of blood types for various countries, I can’t find anything on the general genetics of Rh-factor… though I did notice “Rh-factor” was being called “Type D” is some papers).

Oh, wow… a tweaking of the search terms, and going through a few pages I found a couple of interesting complete articles (I was looking for stuff that was online for free).

First there is this:http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17198846 … in short, D-negativity is complicated (aka Rh-neg)… “D-negative is prevalent in Caucasians (15%-17%), but less common in Black Africans (5%) and Asians (3%).21 The D-negative phenotype has arisen numerous times, and multiple genetic events are responsible for loss of RhD expression in different populations. Caucasians have a deletion of the entire RHD gene,22 but Africans and Asians often have an inactive or silent RHD. Approximately 66% of South African, D-negative, Black persons have RHD with a 37-bp internal duplication that causes a premature stop codon and does not encode functional protein, while 15% carry a hybrid RHD-CE-D.23 This hybrid D-CE-D does not express D antigen and encodes an altered C antigen (Fig. 4B). In Asians, 10-30% of D-negative phenotypes are Del and have very low levels of D antigen not detectable by standard typing (see below).”

Then, this very weird on showed up on Chimera syndrome:http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17330063 … “In 2001, transfusion medicine specialist Willy Flegel and colleagues at the University Hospital in Ulm, Germany, reported on a chimeric blood donor whose mixed blood had transformed the RhD antibody profiles in some transfusion recipients “… a very rare but weird result.

My concerns are related to the group selection and analysis of confounders BUT I do not think that a direct correlation should exist because this is ONE of SEVERAL potential problems ; why in a multicausal condition when the problem is the sinergy of different exposures at different times-prenatal and postnatal. you are going to find a (clear) link with only one-especially if you do not know before if this is a major contributor?
For example
a-There is no information on the families of the mothers immunized with rhoGAM about familiar antecedents of autoimmunity- of autistic and no autistic children. Now, what percentage of mothers of non autistic children have familiar antecedents of autoimmunity and what percentage of the mothers of autistic children have familiar antecedents of autoimmunity? The groups should be similar in composition for the numbers to be comparable. Of course, the RhoGam Inmunoglobulin does its work, the problems is that it is not known the mechanism.Link

The final product contains approximately 5 ± 1% gamma globulin, 2.9 mg/mLsodium chloride, 0.01% polysorbate 80 and 15 mg/mL glycine. Small amounts
of IgA, typically less than 15 ?g per dose, are present.9 The pH range is 6.20-6.55.
The product contains no preservative and utilizes a latex-free delivery system.

b-The RhoGAM of this link has no thimerosal declared. IS there some difference in the numbers of mothers RH negative that have had children who later were diagnosed with ASD when thimerosal was in the RhoGAM than when it is absent –after 2002-, considering the autoimmunity antecedents in the analysis?Where is the comparison between the mothers with autistic children and non-autistic children AFTER 2002 who received thimerosal free?
c-Were there concomitant exposures that could be related to predispostition to autism ( for example terbutalin use) or other exposures that could be concomitant (valproic acid) or viral/bacterian infections during the pregnancy in both groups that could be confounders?
d-Were there concomitant exposures to other xenobiotics?
e-How many mothers got the flu vaccines in both groups, considering the subgroup of mothers with antecedents of autoimmunity in both groups- even when no clinical manifestations of?
f-How many mothers got the tetanus vaccine before delivery- also analyzed by subgroups?
Now, without all these clarifications nothing can be concluded because there are more unknown that controlled variables and we do not know if the groups are comparable. Now let´s see
Lack of association between Rh status, Rh immune globulin in pregnancy and autism.Link

Between 2004 and 2006, 305 mothers of 321 children with an ASD agreed to participate in a telephone interview. Analysis of complete records including the blood group status and RhIg exposure of 214 families showed that Rh(-) status is no higher in mothers of children with autism than in the general population, exposure to antepartum RhIg, preserved with thimerosal is no higher for children with autism and pregnancies are no more likely to be Rh incompatible. This was also true for autism subgroups defined by behavioral phenotype, gender, IQ, regressive onset, head circumference, dysmorphology, birth status, essential, or complex phenotype. [my comment no autoimmune antecedents were listed, no posnatal exposures to thimerosal were analyzed]These findings support the consensus that exposure to ethylmercury in thimerosal is not the cause of the increased prevalence of autism. These data are important not only for parents in this country but also for the international health community where thimerosal continues to be used to preserve multi-dose vials which in turn makes vaccines affordable.

Now, this manuscript was a telephon interview. I remember how other telephon interview…But that is other history . However, this is also a telephon interview.

My concerns are related to the group selection and analysis of confounders BUT I do not think that a direct correlation should exist because this is ONE of SEVERAL potential problems

If something is a significant risk factor, then there should be a way to determine it’s a risk factor; e.g. through a case-control study like Croen et al. It doesn’t really matter if there are thousands of other risk factors.

What are the potential confounds in Croen et al. that you feel would tend to skew the results in favor of the null hypothesis?

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